المؤلفون: Soranzo, N, Sanna, S, Wheeler, E, Gieger, C, Radke, D, Dupuis, J, Bouatia-Naji, N, Langenberg, C, Prokopenko, I, Stolerman, E, Sandhu, MS, Heeney, MM, Devaney, JM, Reilly, MP, Ricketts, SL, Stewart, AF, Voight, BF, Willenborg, C, Wright, B, Altshuler, D, Arking, D, Balkau, B, Barnes, D, Boerwinkle, E, Böhm, B, Bonnefond, A, Bonnycastle, LL, Boomsma, DI, Bornstein, SR, Böttcher, Y, Bumpstead, S, Burnett-Miller, MS, Campbell, H, Cao, A, Chambers, J, Clark, R, Collins, FS, Coresh, J, De Geus, EJ, Dei, M, Deloukas, P, Döring, A, Egan, JM, Elosua, R, Ferrucci, L, Forouhi, N, Fox, CS, Franklin, C, Franzosi, MG, Gallina, S, Goel, A, Graessler, J, Grallert, H, Greinacher, A, Hadley, D, Hall, A, Hamsten, A, Hayward, C, Heath, S, Herder, C, Homuth, G, Hottenga, JJ, Hunter-Merrill, R, Illig, T, Jackson, AU, Jula, A, Kleber, M, Knouff, CW, Kong, A, Kooner, J, Köttgen, A, Kovacs, P, Krohn, K, Kühnel, B, Kuusisto, J, Laakso, M, Lathrop, M, Lecoeur, C, Li, M, Loos, RJ, Luan, J, Lyssenko, V, Mägi, R, Magnusson, PK, Mälarstig, A, Mangino, M, Martínez-Larrad, MT, März, W, McArdle, WL, McPherson, R, Meisinger, C, Meitinger, T, Melander, O, Mohlke, KL, Mooser, VE, Morken, MA, Narisu, N, Nathan, DM, Nauck, M, O'Donnell, C, Oexle, K, Olla, N, Pankow, JS, Payne, F, Peden, JF, Pedersen, NL, Peltonen, L, Perola, M, Polasek, O, Porcu, E, Rader, DJ, Rathmann, W, Ripatti, S, Rocheleau, G, Roden, M, Rudan, I, Salomaa, V, Saxena, R, Schlessinger, D, Schunkert, H, Schwarz, P, Seedorf, U, Selvin, E, Serrano-Ríos, M, Shrader, P, Silveira, A, Siscovick, D, Song, K, Spector, TD, Stefansson, K, Steinthorsdottir, V, Strachan, DP, Strawbridge, R, Stumvoll, M, Surakka, I, Swift, AJ, Tanaka, T, Teumer, A, Thorleifsson, G, Thorsteinsdottir, U, Tönjes, A, Usala, G, Vitart, V, Völzke, H, Wallaschofski, H, Waterworth, DM, Watkins, H, Wichmann, HE, Wild, SH, Willemsen, G, Williams, GH, Wilson, JF, Winkelmann, J, Wright, AF, WTCCC, Zabena, C, Zhao, JH, Epstein, SE, Erdmann, J, Hakonarson, HH, Kathiresan, S, Khaw, KT, Roberts, R, Samani, NJ, Fleming, MD, Sladek, R, Abecasis, G, Boehnke, M, Froguel, P, Groop, L, McCarthy, MI, Kao, WH, Florez, JC, Uda, M, Wareham, NJ, Barroso, I, Meigs, JB

مصطلحات موضوعية: Adult, Blood Glucose, Hemoglobin A, Glycosylated, Male, WTCCC, endocrine system diseases, European Continental Ancestry Group, nutritional and metabolic diseases, Chromosome Mapping, Genetic Variation, 11 Medical And Health Sciences, Middle Aged, Polymorphism, Single Nucleotide, Body Mass Index, Cohort Studies, Endocrinology & Metabolism, Meta-Analysis as Topic, Humans, Female, Genome-Wide Association Study

الوصف: OBJECTIVE - Glycated hemoglobin (HbA1c), used to monitor and diagnose diabetes, is influenced by average glycemia over a 2- to 3-month period. Genetic factors affecting expression, turnover, and abnormal glycation of hemoglobin could also be associated with increased levels of HbA 1c. We aimed to identify such genetic factors and investigate the extent to which they influence diabetes classification based on HbA1c levels. RESEARCH DESIGN AND METHODS - We studied associations with HbA 1c in up to 46,368 nondiabetic adults of European descent from 23 genome-wide association studies (GWAS) and 8 cohorts with de novo genotyped single nucleotide polymorphisms (SNPs). We combined studies using inverse-variance meta-analysis and tested mediation by glycemia using conditional analyses. We estimated the global effect of HbA1c loci using a multilocus risk score, and used net reclassification to estimate genetic effects on diabetes screening. RESULTS - Ten loci reached genome-wide significant association with HbA1c, including six new loci near FN3K (lead SNP/P value, rs1046896/P = 1.6 × 10-26), HFE (rs1800562/P = 2.6 × 10-20), TMPRSS6 (rs855791/P = 2.7 x 10-14), ANK1 (rs4737009/P = 6.1 × 10-12), SPTA1 (rs2779116/P = 2.8 × 10-9) and ATP11A/TUBGCP3 (rs7998202/P = 5.2 × 10 -9), and four known HbA1c loci: HK1 (rs16926246/P = 3.1 × 10-54), MTNR1B (rs1387153/P = 4.0 × 10-11), GCK (rs1799884/P = 1.5 × 10-20) and G6PC2/ABCB11 (rs552976/P = 8.2 × 10-18). We show that associations with HbA1c are partly a function of hyperglycemia associated with 3 of the 10 loci (GCK, G6PC2 and MTNR1B). The seven nonglycemic loci accounted for a 0.19 (% HbA 1c) difference between the extreme 10% tails of the risk score, and would reclassify ∼2% of a general white population screened for diabetes with HbA1c. CONCLUSIONS - GWAS identified 10 genetic loci reproducibly associated with HbA1c. Six are novel and seven map to loci where rarer variants cause hereditary anemias and iron storage disorders. Common variants at these loci likely influence HbA1c levels via erythrocyte biology, and confer a small but detectable reclassification of diabetes diagnosis by HbA1c. © 2010 by the American Diabetes Association.

URL الوصول: https://explore.openaire.eu/search/publication?articleId=od______1032::bc5be7acb3ed4667c3bb7b525d77031a
http://hdl.handle.net/10044/1/28756

المؤلفون: Holstein A, Patzer OM, Machalke K, Holstein JD, Stumvoll M, Kovacs P, Holstein, Andreas, Patzer, Olaf M, Machalke, Kathrin, Holstein, Judith D, Stumvoll, Michael, Kovacs, Peter

المصدر: Diabetes Care; May2012, Vol. 35 Issue 5, p972-975, 4p

مستخلص: Objective: To compare the incidences of severe hypoglycemia and corresponding clinical circumstances in a German population between 2007-2010 and 1997-2000.Research Design and Methods: A screening for severe hypoglycemia was performed in the Lippe-Detmold area in Germany to sensitively detect severe hypoglycemia. This was defined as a symptomatic event requiring treatment with intravenous glucose and being confirmed by a blood glucose measurement of <50 mg/dL.Results: Severe hypoglycemia increased considerably from 264 events in 1997-2000 to 495 events in 2007-2010, which translated into an increase in frequency of severe hypoglycemia among all emergency admissions from 0.68 to 0.83% (P = 0.015). This was mostly related to intensification of antihyperglycemic therapy, particularly in the increasingly morbid group of hypoglycemic patients with type 2 diabetes indicated by lower HbA(1c), more comedication (3.3 vs. 7.7 drugs), and more concomitant diseases (3.6 vs. 4.4) (all P values <0.001).Conclusions: Within a 10-year period, there was an intensification of antihyperglycemic therapy in increasingly comorbid subjects, leading to a considerably higher incidence of severe hypoglycemia. [ABSTRACT FROM AUTHOR]

: Copyright of Diabetes Care is the property of American Diabetes Association and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: Tönjes A, Scholz M, Loeffler M, Stumvoll M

المصدر: Diabetes Care; Nov2006, Vol. 29 Issue 11, p2489-2497, 9p

مستخلص: OBJECTIVE: The provariant of the Pro12Ala polymorphism in peroxisome proliferator-activated receptor (PPAR)gamma has been identified as a risk allele for type 2 diabetes. The purpose of the present study was to reveal a significant association with pre-diabetic phenotypes in nondiabetic individuals based on a systematic meta-analysis of all available published evidence. RESEARCH DESIGN AND METHODS: We performed a classical meta-analysis of data from approximately 32,000 nondiabetic subjects in 57 studies to assess the effect of the Pro12Ala polymorphism on pre-diabetic traits. RESULTS: In the global comparison, there were no differences in BMI, glucose, insulin, or homeostasis model assessment of insulin resistance between the Pro/Pro and X/Ala genotype. However, in the Caucasian subgroup, the X/Ala genotype was associated with significantly increased BMI. In the obese subgroup (BMI >30 kg/m(2)), fasting glucose (P = 0.041) and insulin resistance (by homeostasis model analysis) (P = 0.020) were significantly greater in the Pro/Pro group. In subjects with the homozygous Ala/Ala genotype, fasting insulin was significantly lower compared with the Pro/Pro genotype (P = 0.040, N(Ala/Ala) = 154). CONCLUSIONS: Across all studies, the Pro12Ala polymorphism had no significant effect on diabetes-related traits. Only in selected subgroups, such as Caucasians and obese subjects, did we see an association of the Ala allele with greater BMI and greater insulin sensitivity. This demonstrates the importance for appropriate stratification of analyses by environmental or other genetic factors. Meta-analysis of Ala/Ala homozygotes more clearly demonstrated the association with greater insulin sensitivity of carriers of the Ala allele. [ABSTRACT FROM AUTHOR]

: Copyright of Diabetes Care is the property of American Diabetes Association and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: Bachmann, Oliver P., Dahl, Dominik B., Brechtel, Klaus, Machann, Jurgen, Haap, Michael, Maier, Thomas, Loviscach, Mattias, Stumvoll, Michael, Claussen, Claus D., Schick, Fritz, Haring, Hans U., Jacob, Stephan, Bachmann, O P, Dahl, D B, Brechtel, K, Machann, J, Haap, M, Maier, T, Loviscach, M, Stumvoll, M

المصدر: Diabetes; Nov2001, Vol. 50 Issue 11, p2579-2584, 6p, 2 Charts, 4 Graphs

مصطلحات موضوعية: LIPID metabolism, INSULIN, MUSCLES

مستخلص: An increased intramyocellular lipid (IMCL) content, as quantified by (1)H-magnetic resonance spectroscopy ((1)H-MRS), is associated with reduced insulin sensitivity. At present, it is unclear which factors determine IMCL formation and how rapidly IMCL accumulation can be induced. We therefore studied the impact of hyperinsulinemia and elevated circulating nonesterified fatty acid (NEFA) levels on IMCL formation and insulin sensitivity. We further evaluated the influence of a high-fat diet on IMCL storage. In the infusion protocol, 12 healthy male subjects underwent a 6-h hyperinsulinemic-euglycemic glucose clamp with concomitant infusion of Intralipid plus heparin. IMCL was quantified by (1)H-MRS in soleus (SOL) and tibialis anterior (TA) muscle at baseline and then every hour. IMCL levels started to increase significantly after 2 h, reaching a maximum of 120.8 +/- 3.4% (SOL) and 164.2 +/- 13.8% (TA) of baseline after 6 h (both P < 0.05). In parallel, the glucose infusion rate (GIR) decreased progressively, reaching a minimum of 60.4 +/- 5.4% of baseline after 6 h. Over time, the GIR was strongly correlated with IMCL in TA (r = -0.98, P < or = 0.003) and SOL muscle (r = -0.97, P < or = 0.005). In the diet protocol, 12 male subjects ingested both a high-fat and low-fat diet for 3 days each. Before and after completion of each diet, IMCL levels and insulin sensitivity were assessed. After the high-fat diet, IMCL levels increased significantly in TA muscle (to 148.0 +/- 16.9% of baseline; P = 0.005), but not in SOL muscle (to 114.4 +/- 8.2% of baseline; NS). Insulin sensitivity decreased to 83.3 +/- 5.6% of baseline (P = 0.033). There were no significant changes in insulin sensitivity or IMCL levels after the low-fat diet. The effects of the high-fat diet showed greater interindividual variation than those of the infusion protocol. The data from the lipid infusion protocol suggest a functional relationship between IMCL levels and insulin sensitivity. Similar effects could be induced by a high-fat diet, thereby underlining the physiological relevance of these observations. [ABSTRACT FROM AUTHOR]

: Copyright of Diabetes is the property of American Diabetes Association and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: Stefan, Norbert, Fritsche, Andreas, Haring, Hans, Stumvoll, Michael, Stefan, N, Fritsche, A, Häring, H, Stumvoll, M

المصدر: Diabetes; May2001, Vol. 50 Issue 5, p1143-1148, 6p, 2 Charts, 3 Graphs

مصطلحات موضوعية: INSULIN, HEPARIN, PEROXISOMES, SECRETION

مستخلص: The transcription of many genes involved in lipid metabolism is regulated by the peroxisome proliferator-activated receptor-gamma (PPAR-gamma). The Pro12Ala polymorphism in the PPAR-gamma2 gene has been associated with reduced transcriptional activity in vitro and increased insulin sensitivity in vivo. Although PPAR-gamma has been demonstrated in human beta-cells, it is unknown whether the Pro12Ala polymorphism plays a role in insulin secretion. Moreover, it is also unknown if and how the effect of free fatty acids (FFAs) on insulin secretion and insulin sensitivity is modulated by the presence of this polymorphism. We therefore performed hyperglycemic clamps (8 mmol/l, 140 min, 5 g arginine bolus at min 120) in 10 healthy subjects with the (X/Ala) polymorphism and in 10 subjects without the polymorphism (Pro/Pro) basally and after 5 h infusion of Intralipid plus heparin. FFA concentrations increased from 473 +/- 61 micromol/l to 1,732 +/- 163 micromol/l in the Pro/Pro and from 372 +/- 46 micromol/l to 1,630 +/- 96 micromol/l in the X/Ala group (P = 0.68). Basally, neither insulin sensitivity nor insulin secretion were significantly different between the two groups. During infusion of Intralipid, first-phase insulin secretion remained unchanged in both groups (P = 0.21). In the Pro/Pro group, second-phase insulin secretion remained unchanged (444 +/- 67 vs. 471 +/- 93 pmol/min) and the response to arginine increased from 5,007 +/- 41 to 6,072 +/- 732 pmol/min. In contrast, in the X/Ala group, there was a decrease of both second-phase insulin secretion (533 +/- 58 to 427 +/- 48 pmol/min, P = 0.02 vs. Pro/Pro) and in the response to arginine (from 7,518 +/- 1,306 to 6,458 +/- 1,040 pmol/min, P = 0.014 vs. Pro/Pro). The insulin sensitivity index decreased comparably in Pro/Pro and X/Ala (to 71 +/- 8 vs. 74 +/- 9% of basal, P = 0.8). In conclusion, these results provide evidence that the Pro12Ala polymorphism in the PPAR-gamma2 gene might be involved in a differential regulation of insulin secretion in response to increased FFAs in humans. [ABSTRACT FROM AUTHOR]

: Copyright of Diabetes is the property of American Diabetes Association and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: Stumvoll, Michael, Stumvoll, M, Wahl, H G, Löblein, K, Becker, R, Machicao, F, Jacob, S, Häring, H

المصدر: Diabetes; Apr2001, Vol. 50 Issue 4, p876-881, 6p, 1 Chart, 6 Graphs

مصطلحات موضوعية: GENETIC polymorphisms, INSULIN, LIPOLYSIS

مستخلص: The Pro12Ala polymorphism of the peroxisome proliferator-activated receptor (PPAR)-gamma2 is associated with reduced transcriptional activity in vitro and increased insulin sensitivity in humans in vivo. The mechanism by which this polymorphism influences insulin sensitivity in humans is unclear. PPAR-gamma2 is mainly expressed in adipocytes, and free fatty acids released from adipose tissue are key mediators of peripheral insulin resistance. Therefore, we examined insulin suppression of lipolysis in 51 subjects without (Pro/Pro) and 17 subjects with the polymorphism (X/Ala). Both groups were lean (BMI <27.0 kg/m2) and matched for age, BMI, waist-to-hip ratio, and sex. The isotopically (infusion of d5 glycerol) determined glycerol rate of appearance was used as an index of lipolysis. Insulin sensitivity of lipolysis was expressed as the insulin concentration resulting in half-maximal suppression (EC50). This was directly determined during a three-step hyperinsulinemic-euglycemic clamp (n = 21) or estimated indirectly during a standard hyperinsulinemic-euglycemic clamp (n = 47). The insulin sensitivity index (ISI) of glucose disposal was 0.095+/-0.006 micromol x kg(-1) x min(-1) x pmol(-1) x l(-1) in the control group and 0.129+/-0.008 micromol x kg(-1) x min(-1) x pmol(-1) x l(-1) in the X/Ala group (P = 0.003). The EC50 was 56+/-2 pmol/l in the control group and 44+/-3 pmol/l in the X/Ala group (P = 0.001). The EC50 of lipolysis and ISI was significantly correlated (r = 0.42, P = 0.002). In conclusion, in lean subjects, the Pro12Ala polymorphism is associated with increased insulin sensitivity of glucose disposal and suppression of lipolysis. This result suggests that an altered transcriptional activity of PPAR-gamma2 in X/Ala subjects either causes a more efficient suppression of lipolysis in adipose tissue, which in turn results in improved insulin-stimulated glucose disposal in muscle, or, alternatively, beneficially affects insulin signaling in both tissues independently of one another. [ABSTRACT FROM AUTHOR]

: Copyright of Diabetes is the property of American Diabetes Association and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: Stumvoll, Michael, Stumvoll, M, Fritsche, A, Volk, A, Stefan, N, Madaus, A, Maerker, E, Teigeler, A, Koch, M, Machicao, F, Häring, H

المصدر: Diabetes; Apr2001, Vol. 50 Issue 4, p882-885, 4p, 4 Charts, 3 Graphs

مصطلحات موضوعية: GENETIC polymorphisms, INSULIN, INSULIN resistance, SECRETION

مستخلص: The Gly972Arg polymorphism in the insulin receptor substrate (IRS)-1 was found in some studies to have a higher prevalence in type 2 diabetic subjects than in control subjects. Previously, transfection of IRS-1 with this polymorphism into insulin-secreting cells resulted in a marked reduction of glucose-stimulated insulin secretion compared with the wild-type transfected cells. In the present study, we compared insulin secretion in well-matched normal glucose-tolerant subjects with and without this polymorphism. Several validated indexes of beta-cell function from the oral glucose tolerance test were significantly lower in X/Arg (n = 31) compared with Gly/Gly (n = 181) (P between 0.002 and 0.05), whereas insulin sensitivity (measured with a euglycemic clamp) was not different. During a modified hyperglycemic clamp, insulin secretion rates were significantly lower in Gly/Arg (n = 8) compared with Gly/Gly (n = 36) during the first phase (1,711+/-142 vs. 3,014+/-328 pmol/min, P = 0.05) and after maximal stimulation with arginine (5,340+/-639 vs. 9,075+/-722 pmol/min, P = 0.03). In summary, our results suggest that the Gly972Arg polymorphism in IRS-1 is associated with decreased insulin secretion in response to glucose but not with insulin sensitivity. It is possible that this polymorphism causes insulin resistance at the level of the beta-cell and contributes to the polygenic etiology of type 2 diabetes. [ABSTRACT FROM AUTHOR]

: Copyright of Diabetes is the property of American Diabetes Association and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: Gerich, J E, Meyer, C, Woerle, H J, Stumvoll, M

المصدر: Diabetes Care; Feb2001, Vol. 24 Issue 2, p382-391, 10p

مستخلص: Studies conducted over the last 60 years in animals and in vitro have provided considerable evidence that the mammalian kidney can make glucose and release it under various conditions. Until quite recently however, it was generally believed that the human kidney was not an important source of glucose except during acidosis and after prolonged fasting. This review will summarize early work in animals and humans, discuss methodological problems in assessing renal glucose release in vivo, and present results of recent human studies that provide evidence that the kidney may play a significant role in carbohydrate metabolism under both physiological and pathological conditions. [ABSTRACT FROM AUTHOR]

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المؤلفون: Stumvoll, Michael, Mitrakou, Asimina, Pimenta, Walkyria, Jenssen, Trond, Yki-Jarvinen, Hannele, Van Haeften, Timon, Renn, Walter, Gerich, John, Stumvoll, M, Mitrakou, A, Pimenta, W, Jenssen, T, Yki-Järvinen, H, Van Haeften, T, Renn, W, Gerich, J

المصدر: Diabetes Care; Mar2000, Vol. 23 Issue 3, p295-301, 7p, 4 Graphs

مصطلحات موضوعية: BLOOD sugar, GLUCOSE tolerance tests, INSULIN, PANCREATIC beta cells

مستخلص: Objective: The oral glucose tolerance test (OGTT) has often been used to evaluate apparent insulin release and insulin resistance in various clinical settings. However, because insulin sensitivity and insulin release are interdependent, to what extent they can be predicted from an OGTT is unclear.Research Design and Methods: We studied insulin sensitivity using the euglycemic-hyperinsulinemic clamp and insulin release using the hyperglycemic clamp in 104 nondiabetic volunteers who had also undergone an OGTT. Demographic parameters (BMI, waist-to-hip ratio, age) and plasma glucose and insulin values from the OGTT were subjected to multiple linear regression to predict the metabolic clearance rate (MCR) of glucose, the insulin sensitivity index (ISI), and first-phase (1st PH) and second-phase (2nd PH) insulin release as measured with the respective clamps.Results: The equations predicting MCR and ISI contained BMI, insulin (120 min), and glucose (90 min) and were highly correlated with the measured MCR (r = 0.80, P < 0.00005) and ISI (r = 0.79, P < 0.00005). The equations predicting 1st PH and 2nd PH contained insulin (0 and 30 min) and glucose (30 min) and were also highly correlated with the measured 1st PH (r = 0.78, P < 0.00005) and 2nd PH (r = 0.79, P < 0.00005). The parameters predicted by our equations correlated better with the measured parameters than homeostasis model assessment for secretion and resistance, the delta30-min insulin/delta30-min glucose ratio for secretion and insulin (120 min) for insulin resistance taken from the OGTT.Conclusions: We thus conclude that predicting insulin sensitivity and insulin release with reasonable accuracy from simple demographic parameters and values obtained during an OGTT is possible. The derived equations should be used in various clinical settings in which the use of clamps or the minimal model would be impractical. [ABSTRACT FROM AUTHOR]

: Copyright of Diabetes Care is the property of American Diabetes Association and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: Fritsche, A, Stumvoll, M, Grüb, M, Sieslack, S, Renn, W, Schmülling, R M, Häring, H U, Gerich, J E

المصدر: Diabetes Care; Sep1998, Vol. 21 Issue 9, p1505-1510, 6p